Cold face test demonstrates parasympathetic cardiac dysfunction in familial dysautonomia

1999 ◽  
Vol 276 (6) ◽  
pp. R1833-R1839 ◽  
Author(s):  
M. J. Hilz ◽  
B. Stemper ◽  
P. Sauer ◽  
U. Haertl ◽  
W. Singer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Transfer Function ◽  
Power Spectra ◽  
Familial Dysautonomia ◽  
Cold Face ◽  
Parasympathetic Dysfunction ◽  
Transfer Function Gain ◽  
Cold Face Test

In familial dysautonomia (FD), i.e., Riley-Day syndrome, parasympathetic dysfunction has not been sufficiently evaluated. The cold face test is a noninvasive method of activating trigeminal brain stem cardiovagal and sympathetic pathways and can be performed in patients with limited cooperation. We performed cold face tests in 11 FD patients and 15 controls. For 60 s, cold compresses (0–1°C) were applied to the cheeks and forehead while we monitored heart rate, respiration, beat-to-beat radial artery blood pressure, and laser-Doppler skin blood flow at the first toe pulp. From these measurements heart rate variability parameters were calculated: root mean square of successive differences (RMSSD), coefficient of variation (CV), low- and high-frequency (LF and HF, respectively) power spectra of the electrocardiogram, and the LF transfer function gain between blood pressure and heart rate. All patients perceived cold stimulation and acknowledged discomfort. In controls, heart rate and skin blood flow decreased significantly during cold face test; in patients, both parameters decreased only briefly and not significantly. In controls, blood pressure, RMSSD, CV, and heart rate HF-power spectra increased but remained unchanged in patients. Respiration, as well as heart rate LF power spectra, did not change in either group. In controls, LF transfer function gain between blood pressure and heart rate indicated that bradycardia was not secondary to blood pressure increase. We conclude that the cold face test demonstrated that patients with FD have a reduced cardiac parasympathetic response, which implies efferent parasympathetic dysfunction.

Effects of age, sex, and physical fitness on responses to local cooling

1978 ◽  
Vol 44 (5) ◽  
pp. 813-817 ◽  
Author(s):  
J. LeBlanc ◽  
J. Cote ◽  
S. Dulac ◽  
F. Dulong-Turcot
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Physical Fitness ◽  
Female Group ◽  
Local Cooling ◽  
Trained Subjects ◽  
Cold Face ◽  
Hand Test ◽  
Older Subjects ◽  
Cold Face Test

The response to local cooling was estimated by the cold hand test (5 degrees C for 2 min) and the cold face test (0 degrees C with 66 km.h-1 wind for 2 min). Heart rate, blood pressure, and skin temperature were measured before, during, and after the tests. The increase in blood pressure (cold hand test) and the fall in Tsk (cold face test) were reduced in trained subjects. Similarly older subjects (53–60 yr of age) responded less to a cold hand test than younger subjects aged 20–40. However, the bradycardia caused by the cold face test was more pronounced in the older subjects. The responses to the cold hand and cold face tests were the same for male and female subjects. During the 2 min after the test, blood pressure and heart rate fell below initial values in the female group but not in the male. It is concluded that, besides adaptation to cold, individual factors such as age, sex, and physical fitness also have a relative importance in the responses to local cooling.

Reduced baroreflex sensitivity in elderly humans is not due to efferent autonomic dysfunction

1999 ◽  
Vol 98 (1) ◽  
pp. 103-110 ◽  
Author(s):  
D. O'MAHONY ◽  
C. BENNETT ◽  
A. GREEN ◽  
A. J. SINCLAIR
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Reflex Response ◽  
Cognitive Stress ◽  
Age Related ◽  
Cold Face ◽  
Blood Pressure Responses ◽  
Age Range ◽  
Cold Face Test

A progressive decline in baroreflex sensitivity (BRS) is a characteristic feature of human aging, the basis of which is poorly understood. The purpose of the present study was to determine whether alterations in efferent baroreflex function might contribute to the age-related decrease in BRS. We studied 10 healthy young (mean age 30.5 years; age range 22–40 years; six male) and 10 healthy elderly (mean age 70.7 years; age range 67–75 years; five male) volunteers. We tested efferent cardiac vagal function using the bradycardiac response to the cold face test, and efferent sympathetic function using heart rate and blood pressure responses to four stress tests: (i) low-level cognitive stress, (ii) high-level cognitive stress, (iii) hand immersion in ice water (cold pressor test) and (iv) isometric sustained hand-grip. Haemodynamic responses to these stresses are mediated via efferent baroreflex pathways, whereas the afferent components of each reflex response are independent of afferent baroreflex pathways. BRS was measured from simultaneous Finapres-derived continuous blood pressure and digital ECG R–R interval data using the sequence analysis paradigm. As expected, BRS was significantly reduced in the elderly group (7.29±0.74 ms/mmHg; mean±S.E.M.) compared with the young group (13.84±1.13 ms/mmHg; P < 0.001). However, neither the bradycardiac responses to the cold face test nor the efferent sympathetically mediated heart rate/blood pressure responses to the stress test battery were significantly different between the young and elderly groups. We conclude that the age-related decrease in BRS is not attributable to impairments in the efferent sympathetic or parasympathetic system components of the baroreceptor reflex pathway.

Dynamic autoregulation of cutaneous circulation: differential control in glabrous versus nonglabrous skin

2005 ◽  
Vol 289 (1) ◽  
pp. H385-H391 ◽  
Author(s):  
Thad E. Wilson ◽  
Rong Zhang ◽  
Benjamin D. Levine ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Transfer Function ◽  
Skin Blood Flow ◽  
Neural Control ◽  
Spectral Power ◽  
Frequency Range ◽  
Pressure Oscillations ◽  
Ganglionic Blockade ◽  
Transfer Function Gain

The purpose of this project was to test the hypothesis that, independent of neural control, glabrous and nonglabrous cutaneous vasculature is capable of autoregulating blood flow. In 10 subjects, spectral and transfer function analyses of arterial pressure and skin blood flow (laser-Doppler flowmetry) from glabrous (palm) and nonglabrous (forearm) regions were performed under three conditions: baseline, ganglionic blockade via intravenous trimethaphan administration, and trimethaphan plus oscillatory lower body negative pressure (LBNP; −5 to −10 mmHg) from 0.05 to 0.07 Hz. Oscillatory LBNP was applied to regenerate mean arterial pressure variability that was abolished by ganglionic blockade. Ganglionic blockade was verified by an absence of a heart rate response to a Valsalva maneuver. Spectral power and transfer function gain between blood pressure and skin blood flow were calculated in this oscillatory frequency range (0.05–0.07 Hz). Within this frequency range, ganglionic blockade significantly decreased spectral power of blood flow in both the forearm and palm, whereas regeneration of arterial blood pressure oscillations significantly increased spectral power of forearm blood flow but not palm blood flow. During oscillatory LBNP, transfer function gain between blood pressure and skin blood flow was significantly elevated at the forearm (0.28 ± 0.03 to 0.53 ± 0.02 flux units/mmHg; P < 0.05) but was reduced at the palm (4.7 ± 0.5 to 1.2 ± 0.1 flux units/mmHg; P < 0.05). These data show that independent of neural control of blood flow, glabrous skin has the ability to buffer blood pressure oscillations and demonstrates a degree of dynamic autoregulation. Conversely, these data suggest that nonglabrous skin has diminished dynamic autoregulatory capabilities.

Blood pressure, heart rate, and adrenal catecholamines prior to ventricular fibrillation

1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Ventricular Fibrillation ◽  
Coronary Occlusion ◽  
Marked Decrease ◽  
Mean Blood Pressure ◽  
Plasma Adrenaline ◽  
Acute Coronary Occlusion ◽  
Before And After

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.

Hypothalamic paraventricular nucleus is critical for renal vasoconstriction elicited by elevations in body temperature

2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Core Temperature ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Body Core Temperature ◽  
Control Group ◽  
Body Core

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

scholarly journals Acute, local infusion of angiotensin II impairs microvascular and metabolic insulin sensitivity in skeletal muscle

2018 ◽  
Vol 115 (3) ◽  
pp. 590-601 ◽  
Author(s):  
Dino Premilovac ◽  
Emily Attrill ◽  
Stephen Rattigan ◽  
Stephen M Richards ◽  
Jeonga Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Microvascular Blood Flow ◽  
Euglycaemic Clamp ◽  
Hyperinsulinaemic Euglycaemic Clamp ◽  
Skeletal Muscle Glucose Uptake

Abstract Aims Angiotensin II (AngII) is a potent vasoconstrictor implicated in both hypertension and insulin resistance. Insulin dilates the vasculature in skeletal muscle to increase microvascular blood flow and enhance glucose disposal. In the present study, we investigated whether acute AngII infusion interferes with insulin’s microvascular and metabolic actions in skeletal muscle. Methods and results Adult, male Sprague-Dawley rats received a systemic infusion of either saline, AngII, insulin (hyperinsulinaemic euglycaemic clamp), or insulin (hyperinsulinaemic euglycaemic clamp) plus AngII. A final, separate group of rats received an acute local infusion of AngII into a single hindleg during systemic insulin (hyperinsulinaemic euglycaemic clamp) infusion. In all animals’ systemic metabolic effects, central haemodynamics, femoral artery blood flow, microvascular blood flow, and skeletal muscle glucose uptake (isotopic glucose) were monitored. Systemic AngII infusion increased blood pressure, decreased heart rate, and markedly increased circulating glucose and insulin concentrations. Systemic infusion of AngII during hyperinsulinaemic euglycaemic clamp inhibited insulin-mediated suppression of hepatic glucose output and insulin-stimulated microvascular blood flow in skeletal muscle but did not alter insulin’s effects on the femoral artery or muscle glucose uptake. Local AngII infusion did not alter blood pressure, heart rate, or circulating glucose and insulin. However, local AngII inhibited insulin-stimulated microvascular blood flow, and this was accompanied by reduced skeletal muscle glucose uptake. Conclusions Acute infusion of AngII significantly alters basal haemodynamic and metabolic homeostasis in rats. Both local and systemic AngII infusion attenuated insulin’s microvascular actions in skeletal muscle, but only local AngII infusion led to reduced insulin-stimulated muscle glucose uptake. While increased local, tissue production of AngII may be a factor that couples microvascular insulin resistance and hypertension, additional studies are needed to determine the molecular mechanisms responsible for these vascular defects.

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